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Construction of Model Lipid Membranes Incorporating G-protein Coupled Receptors (GPCRs)
Published on: February 5, 2022
The interactivities with lipid membranes differentially characterize selective and nonselective beta1-blockers
Maki Mizogami1, Ko Takakura, Hironori Tsuchiya
1Department of Anesthesiology, Asahi University School of Dentistry, Gifu, Japan. makikai@dent.asahiu.ac.jp
European Journal of Anaesthesiology
|July 6, 2010
Summary
Nonselective beta-blockers, unlike selective beta1-blockers, alter cell membrane fluidity. This membrane fluidization is linked to their hydrophobicity and may contribute to nonselective beta-adrenoceptor blockade.
Area of Science:
- Pharmacology
- Biophysics
- Membrane Biology
Background:
- Beta-adrenoceptor-blocking agents are crucial for perioperative management in anesthesia.
- Selective beta1-blockers offer advantages over nonselective beta-blockers.
- Differential interaction of beta1-blockers with lipid membranes is a key characteristic.
Purpose of the Study:
- To comparatively analyze the membrane interactivities of selective and nonselective beta-blockers.
- To evaluate the potency of beta-blockers in modifying membrane fluidity.
- To assess the relative hydrophobicities of different beta-blockers.
Main Methods:
- Reaction of selective (atenolol, metoprolol, esmolol) and nonselective (alprenolol, oxprenolol, propranolol) beta-blockers with liposomes and biomimetic membranes.
- Determination of membrane interactivity via fluorescence polarization to measure membrane fluidity.
- Evaluation of relative hydrophobicities using reversed-phase liquid chromatography.
Main Results:
- Chromatographic analysis separated beta-blockers into more hydrophobic (nonselective) and less hydrophobic (selective beta1) groups.
- Nonselective beta-blockers fluidized liposomal membranes; selective beta1-blockers did not.
- The potency of membrane fluidization by nonselective beta-blockers followed the order: oxprenolol < alprenolol < propranolol.
Conclusions:
- Membrane-fluidizing effects correlate with beta-blocker hydrophobicity and their ability to perturb phospholipid acyl chains.
- Distinct membrane interaction profiles differentiate nonselective (propranolol, alprenolol, oxprenolol) from selective beta1-blockers (atenolol, metoprolol, esmolol).
- Membrane fluidization may partially explain the mechanism of nonselective beta-adrenoceptor blockade.
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